Reference: Hara S, et al. (2021) Dectin-1-mediated suppression of RANKL-induced osteoclastogenesis by glucan from baker's yeast. J Cell Physiol 236(7):5098-5107

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Abstract


Immunoreceptors expressed on osteoclast precursor cells modify osteoclast differentiation and bone resorption activity. Dectin-1 is a lectin receptor of β-glucan and is specifically expressed in osteoclast precursor cells. In this study, we evaluated the bioactivity of β-glucan on receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis and observed that glucan from baker's yeast inhibited this process in mouse bone marrow cells and dectin-1-overexpressing RAW264.7 (d-RAW) cells. In conjunction, RANKL-induced nuclear factor of activated T cell c1 expression was suppressed, subsequently downregulating TRAP and Oc-stamp. Additionally, nuclear factor-kappa B activation and the expression of c-fos and Blimp1 were reduced in d-RAW cells. Furthermore, glucan from baker's yeast induced the degradation of Syk protein, essential factor for osteoclastogenesis. These results suggest that glucan from baker's yeast suppresses RANKL-induced osteoclastogenesis and can be applied as a new treatment strategy for bone-related diseases.

Reference Type
Journal Article | Research Support, Non-U.S. Gov't
Authors
Hara S, Nagai-Yoshioka Y, Yamasaki R, Adachi Y, Fujita Y, Watanabe K, Maki K, Nishihara T, Ariyoshi W
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